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The Neuromuscular Junction in Health and Disease

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The Neuromuscular Junction in Health and Disease THE NEUROMUSCULAR JUNCTION IN HEALTH AND DISEASE Biomedical Seminar Room 7, Mondays 9:30-11:30 a lifetime, a part; neuro-muscular junctions: mind meeting matter. We can’t live without our neuromuscular junctions (NMJ’s). Thousands of motor neurones each supply an axon branch that delivers hundreds of motor nerve terminals to our skeletal muscle fibres. Each terminal arbor forms synapses on the surface of a single muscle fibre at a single patch, about 400 µm2 in area and each of these motor endplates is endowed with tens of millions (about 105/µm2) of ligand-gated acetylcholine receptors and voltage- gated sodium ion channels. High-fidelity synaptic transmission and homeostatic, synaptic strength-regulating mechanisms empower NMJ’s, enabling them to activate skeletal muscles with an extraordinary degree of reliability; thus enabling a myriad of delicate-to- intense voluntary movements, thereby linking cognition and intention to behaviour. When these highly-tuned, impedance-matched nerve-muscle connections fail, as they may do with advancing age or disrepair - or as a result of injury, poisoning or disease – affected individuals may suffer symptoms and show signs of severe motor disturbances, ranging from painful seizures or cramps to weakness or complete paralysis. In fact, respiratory paralysis - due to failure of neuromuscular junctions - is a critical feature in illnesses or infections, such as myasthenia gravis or botulism, respectively; and degeneration of NMJ’s in respiratory muscle is a harbinger of death in incurable motor neurone diseases such as amyotrophic lateral sclerosis (ALS). Injuries to peripheral nerves can also be highly debilitating, triggering “Wallerian” degeneration of axons and motor nerve terminals disconnected from their cell bodies, which leads to partial or complete denervation and paralysis of muscle fibres. Fortunately, injured peripheral nerve axons are capable of successful regeneration, unlike most axons in the Central Nervous System (CNS), which further adds to the value of studying mechanisms of peripheral nerve repair: since a deeper understanding of these mechanisms could have an impact on the quest to find ways to repair damaged axons more effectively in the brain and spinal cord. The structure of neuromuscular synapses, as one might expect, is intimately entwined with their function. Drugs that act selectively on neuromuscular transmission, influencing either the release of acetylcholine from nerve terminals or the action of these molecules on postsynaptic receptors, play important roles both in revealing the normal function of these synapses and in treatment for neuromuscular disorders. Homeostatic mechanisms regulate the size and strength of neuromuscular connections and ensure a high margin of ‘safety’ for neuromuscular transmission, ensuring reliability of movement and behaviour. During development, the exquisite interplay of the different molecular and cellular components of neuromuscular synapses lies somewhere between and akin to the co-operativity of an intimate love-affair and the competitive struggle of all-out war. These mechanisms are at least partly activity-dependent, implying the presence of Hebbian ‘use-it-lose-it’ mechanisms, with respect to strength and maintenance of synaptic connections. Similar processes - and perhaps similar molecules - regulate the repair of damaged connectivity and these processes are important targets for developing more effective treatments for neurodegenerative diseases such as ALS. Finally, in addition to the synaptic connections between motor neurone terminals and the motor end-plates of muscle fibres, we now know that two kinds of supporting cells, terminal Schwann cells and kranocytes, co-exist at NMJ’s and co-operate in their formation, maintenance and plasticity. Structure of the NMJiHaD course The NMJiHaD course comprises five “mini-symposia”, prepared and delivered by student members of the class. Each symposium focuses on a different aspect of the structure, function, development and plasticity of neuromuscular synaptic connections and their relevance to the understanding of disease or injury affecting motor neurones. Thus, the course is not comprehensive and several areas of interest are not covered or touched on in a limited way. (For example, we do not dwell very much on the biochemistry or pharmacology of neuromuscular junctions). However, the topics we do cover will include discussion of cutting-edge research. 1 The class will be divided into five groups (“Motor Units”), each with four or five members and each group will be responsible for delivering one of the mini-symposia. Four members of the group (“Motor Nerve Terminals”) will deliver 15-20 minute presentations of the research papers that illustrate the topic (one paper per presenting student). The fifth member of the group (the “Axon”) will Chair the mini-symposium. As well as steering questions from the audience, the Chairperson should also think of questions to ask each speaker. This is a valuable generic skill for anyone chairing a meeting: it is quite often necessary for the chair to get the ball rolling, or to maintain the momentum of discussion when audience members or other attendees appear reticent. The Chair shall also be a rapporteur, responsible for summarizing their mini-symposium and writing a brief (2-page) overview of all the papers presented, for circulation to the class. The mini-symposia will be held in alternate weeks. In the interleaving weeks, the session will normally begin with an introduction to the topic of the next mini-symposium by the course organiser (RRR: the “Soma”), followed by a discussion of the Abstracts of the papers to be presented by one of the groups the following week. The format of these group discussions will be structured as follows: 1. Each abstract is read aloud by a member of the group 2. The Group identifies, defines and clarifies any difficult terms or terminology 3. The Group freely discusses the issues raised by the paper 4. Each group decides on up to four “burning questions” (BQ’s) from the issues discussed 5. In plenary discussion, the class narrows down the number of BQ’s to four “Big Burning Questions” (BBQ’s) that the presenting group should endeavour to address in the following week’s mini-symposium. Mini-symposium topics : I. Structure and function of neuromuscular junctions II. Physiology and pathophysiology of neuromuscular transmission III. Development, Degeneration and Repair of the NMJ IV. Activity-dependent plasticity of NMJ V. The NMJ in Motor Neurone Disease Introductory talks (RRR unless otherwise indicated*) Week Topic 1. Overview of course structure; MCQ revision of NMJ; review of anatomy and physiology of the NMJ; 3. Quantal analysis and the ‘safety-factor’ for neuromuscular transmission 5. Neuromuscular synapse formation, elimination and regeneration 8. Activity-dependent plasticity of the NMJ (*Rosalind Brown) 10. Involvement of the NMJ in Motor Neurone Disease 2 General Reading Byrne, JH & Roberts, JL (2009) From Molecules to Networks 2nd edn. Sinauer. Chapters 2, 5, 8,11,13,16, 20 Katz B. Neural transmitter release: from quantal secretion to exocytosis and beyond.. J Neurocytol. 2003 Jun-Sep;32(5-8):437-46. PMID: 15034246 Sanes JR, Lichtman JW. Development of the vertebrate neuromuscular junction. Annu Rev Neurosci. 1999;22:389-442. PMID: 10202544 Hughes BW, Kusner LL, Kaminski HJ. Molecular architecture of the neuromuscular junction. Muscle Nerve. 2006 Apr;33(4):445-61. PMID: 16228970 Ribchester RR. Mammalian neuromuscular junctions: modern tools to monitor synaptic form and function. Curr Opin Pharmacol. 2009 Jun;9(3):297-305. PMID: 19394273 RRR’s Top Ten NMJ Papers 1: Fatt P, Katz B. Spontaneous subthreshold activity at motor nerve endings. J Physiol. 1952 May;117(1):109-28.PMID: 14946732 2: Boyd IA, Martin AR. The end-plate potential in mammalian muscle. J Physiol. 1956 Apr 27;132(1):74-91. PMID: 13320373 3: Dodge FA Jr, Rahamimoff R.Co-operative action a calcium ions in transmitter release at the neuromuscular junction. J Physiol. 1967 Nov;193(2):419-32. PMID: 6065887 4: Brown MC, Jansen JK, Van Essen D. Polyneuronal innervation of skeletal muscle in new-born rats and its elimination during maturation. J Physiol. 1976 Oct;261(2):387-422. PMID: 978579 5: McLachlan EM, Martin AR. Non-linear summation of end-plate potentials in the frog and mouse. J Physiol. 1981 Feb;311:307-24. PMID: 6267255 6: Mishina M, Takai T, Imoto K, Noda M, Takahashi T, Numa S, Methfessel C, Sakmann B. Molecular distinction between fetal and adult forms of muscle acetylcholine receptor. Nature. 1986 May 22-28;321(6068):406-11. PMID: 2423878 7: Betz WJ, Bewick GS. Optical analysis of synaptic vesicle recycling at the frog neuromuscular junction. Science. 1992 Jan 10;255(5041):200-3. PMID: 1553547. 8: Wood SJ, Slater CR. The contribution of postsynaptic folds to the safety factor for neuromuscular transmission in rat fast- and slow-twitch muscles. J Physiol. 1997 Apr 1;500 ( Pt 1):165-76. PMID: 9097941 9: Harlow ML, Ress D, Stoschek A, Marshall RM, McMahan UJ. The architecture of active zone material at the frog's neuromuscular junction. Nature. 2001 Jan 25;409(6819):479-84. PMID: 11206537 10: Walsh MK, Lichtman JW. In vivo time-lapse imaging of synaptic takeover associated with naturally occurring synapse elimination. Neuron. 2003 Jan 9;37(1):67-73. PMID: 12526773 3 MCQ : Knowledge Review/Revision of the Neuromuscular System 1. The following are part of the descending motor pathway EXCEPT: A. Muscle spindles B. The motor cortex C. Upper motor neurones D. Motor neurone pools E. Lower motor neurones 2. Alpha motor neurones may receive synaptic inputs from the following EXCEPT: A. Afferent fibres from muscle spindles B. Spinal interneurones C. Gamma motor neurones D. Upper motor neurones E. Group Ia afferent fibres 3. In muscle innervation by lower motor neurones the following is true EXCEPT: A. Efferent axons exit the spinal cord via the ventral root B. Alpha motor neurones are responsible for the generation of muscle force C.
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